Helicobacter colonization and histopathological profile of chronic gastritis in patients with or without dyspepsia, mucosal erosion and peptic ulcer: A morphological approach to the study of ulcerogenesis in man

Abstract

Helicobacter pylori colonization and the incidence, severity, activity and topography of gastritis were investigated systematically in antrum and corpus mucosal biopsies of 1177 subjects undergoing endoscopy in the absence of gastric complaints (asymptomatic, 49) or for non-ulcer dyspepsia (NUD; 631 patients, 72 of whom had gastric and/or duodenal erosions), active gastric ulcer (GU, 76 patients), active duodenal ulcer (DU, 138 patients), and healed gastric (HGU, 39 cases) or duodenal ulcer (HDU, 230 cases). In the antrum, H. pylori colonization and the incidence, severity and activity of gastritis increased progressively in the sequence asymptomatic, erosion-free NUD, erosive NUD, healed ulcer and active ulcer. The same trend was observed in the corpus as regards H. pylori and gastritis incidence, whereas the severity and activity of gastritis were lower in active DU and erosive NUD and higher in active, proximal GU than in the remaining patients. Active DU and erosive NUD showed the highest incidence of non-atrophic gastritis and lowest type-A or AB atrophic gastritis, while active GU had lowest normal mucosa or type-A gastritis and highest type-B atrophic gastritis. In conclusion, H. pylori colonization and gastritis incidence, severity and, especially, activity of the antrum might all contribute to mucosal erosion and ulceration, whereas the same factors, at least in part and with the exception of proximal GU, seem to have a preventive role when affecting corpus mucosa.

Cellular vacuoles induced by Helicobacter pylori originate from late endosomal compartments.

“…Extensive cell vacuolation is consistently observed in the stomach epithelial layer of H. pylori-infected human gastric ulcer biopsies (4). Extracts of pathogenic strains ofH.…”

“…pylori induce the formation of vacuoles in the cytoplasm ofdifferent cell lines. This vacuolation leads to cell and tissue necrosis, which is believed to play a central role in the establishment of the inflammation of the gastric mucosa by recruiting polimorphonuclear leukocytes (2)(3)(4)(5)(6)(7).…”

“…Biopsies of H. pylori-colonized stomach epithelium show cellular swelling, expansion of endosomal compartments, and extensive vacuolation (4). A vacuolar degeneration of epithelial cells, followed by cell death, is induced in vitro by H. pylori bacterial extracts (5)(6)(7).…”

“…The luminal pH of these vacuoles is acidic, as deduced from the uptake of neutral red, a membrane-permeant amine that becomes protonated in the vacuolar lumen, and from the potentiating effect of ammonia (8). Two virulence factors, produced by pathogenic strains of H. pylori are thought to be mainly responsible for this cell degeneration and death: a urease and a cytotoxin (3,4,7,8). The urease hydrolyzes urea and the ammonia produced permeates membranes, as neutral red does, and accumulates as ammonium ions inside intracellular acidic compartments, thus causing their osmotic swelling (9)(10)(11).…”

Na+,K+‐ATPase of gastric cells A target of Helicobacter pylori cytotoxic activity

“…Heticobacter pytori is a Gram-negative bacterium which plays a central role in the etiology of chronic gastritis and peptic ulcer disease [1][2][3]. Recently, H.…”